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Medical Progress

Commotio Cordis
Barry J. Maron, M.D., and N.A. Mark Estes III, M.D. entricular fibrillation and sudden death triggered by a blunt, nonpenetrating, and often innocent-appearing unintentional blow to the chest without damage to the ribs, sternum, or heart (and in the absence of underlying cardiovascular disease) constitute an event known as commotio cordis, which translates from the Latin as agitation of the heart. This term was first used in the 19th century,1-6 although the occurrence of commotio cordis was described earlier, in accounts of the ancient Chinese martial art of Dim Mak (or touch of death), in which blows to the left of the sternum caused sudden death in opponents.7 An absence of structural cardiac injury distinguishes commotio cordis from cardiac contusion, in which high-impact blows result in traumatic damage to myocardial tissue and the overlying thorax. Beginning in the mid-1700s, sporadic accounts of commotio cordis appeared in the medical literature, mostly in the context of workplace accidents,8-10 and through the mid-1990s, the disorder was noted only occasionally in case reports, going largely unrecognized, except by the forensic pathology community and the Consumer Product Safety Commission.6,11-14 Since then, however,1 both the general public and the medical community have become increasingly aware of commotio cordis as an important cause of sudden cardiac death. It occurs primarily in children, adolescents, and young adults, most often during participation in certain recreational or competitive sports, with rare occurrences during normal, routine daily activities.1,2,6,15-19 Continued interest in commotio cordis and its tragic consequences is evident in epidemiologic studies1,2,19 and a number of experimental laboratory investigations.20-35 This review focuses on the available information regarding the clinical profile, proposed mechanisms, and prevention and treatment of commotio cordis.

From the Hypertrophic Cardiomyopathy Center Minneapolis Heart Institute Foundation, Minneapolis (B.J.M.); and the New England Cardiac Arrhythmia Center, Cardiology Division, Tufts University School of Medicine, Boston (N.A.M.E.). Address reprint requests to Dr. Maron at Minneapolis Heart Institute Foundation, 920 E. 28th St., Suite 620, Minneapolis, MN 55407, or at hcm.maron@mhif.org. N Engl J Med 2010;362:917-27.
Copyright 2010 Massachusetts Medical Society.

Incidence
The precise incidence of commotio cordis is unknown because of the absence of systematic and mandatory reporting, but on the basis of data from the National Commotio Cordis Registry in Minneapolis,1,2,17 it is among the most frequent cardiovascular causes of sudden death in young athletes, after hypertrophic cardiomyopathy and congenital coronary-artery anomalies.17,18 Since commotio cordis occurs in a wide variety of circumstances, it has undoubtedly been underreported but it is being recognized with increasing frequency and is probably more common than it is believed to be.

Epidemiol o gy
In addition to episodic case studies,8,12-14,36-44 most specific information concerning the clinical profile of commotio cordis comes from the Minneapolis registry,
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No. of Commotio Cordis Events

Survivors Sudden deaths Competitive sports Recreational sports Routine daily activities

60 50 40 30 20 10 0
10 1115 1620

2125

26

instantaneous, 20% of victims remain physically active for a few seconds after the blow (e.g., continuing to walk, run, skate, throw a ball, or even speak), which may reflect individual tolerance for sustained ventricular tachyarrhythmias. For example, a baseball pitcher struck in the chest by a batted ball was able to retrieve the ball at his feet, successfully complete the play (throwing out the base runner), and then prepare for his next pitch before collapsing. In another instance, a batter was struck by a pitch while attempting to bunt and collapsed only after running to first base.
Competitive Sports

Age at Event (yr)

About 50% of commotio cordis events have been reported in young competitive athletes (mostly Baseball those between 11 and 20 years of age) participatSoftball ing in a variety of organized amateur sports Hockey typically baseball, softball, ice hockey, football, Football or lacrosse who receive a blow to the chest Soccer that is usually (but not always) delivered by a proRecreational sports (N=48) Lacrosse jectile used to play the game. In baseball, for exCompetitive sports Boxing ample, commotio cordis is often triggered when (N=122) Cricket players are struck in the chest by balls that have been pitched, batted, or thrown in a variety of Rugby scenarios (Table 1, Fig. 2). In hockey, defensive Karate players may intentionally use their chests to block Basketball the puck from an opponents high-velocity shot. 0 20 40 60 80 High-school and college lacrosse players (includNo. of Commotio Cordis Events ing goalies with chest protectors) may be at greatFigure 1. Distribution of Commotio Cordis Events According to Age and Activity. er risk for commotio cordis than athletes in other RETAKE: 1st AUTHOR: Maron Panel A shows the distribution of commotio cordis events according to age 2nd sports that involve similarly solid projectiles (e.g., 1 of 3 cases from the National Commotio 3rd and type of FIGURE: activity in 224 Cordis Regisbaseballs).19 Commotio cordis may also result Revised 1,2,19 Panel B shows try recordedARTIST: over the past 15 years. the distribution of MRL from physical contact between competitors. Such SIZE such events according to the particular sport. 4 col chest blows are produced by the shoulder, foreTYPE: Line Combo 4-C H/T 22p3 arm, elbow, leg, foot, or head, as when two outAUTHOR, PLEASE NOTE: Figure has been and type has beencases reset. since its cre- fielders inadvertently collide while tracking a which hasredrawn documented 224 Please check carefully. ation 15 years ago.1,2,19 (Fig. 1). Commotio cordis baseball in the air, or, alternatively, when a hockey JOB: 361xx ISSUE: and 3-11-10 shows a predilection for children adolescents stick is thrust into an opponents chest. (mean age, 159 years; range, 6 weeks to 50 years). According to the registry, 26% of victims were Recreational Sports younger than 10 years of age, and only 9% were Another 25% of commotio cordis events occur in 25 years of age or older. The condition has rarely recreational sports played at home, on the playbeen reported in blacks or in girls or women; ground, or at picnics or other family gatherings. most victims are boys or men (95%) and are white These innocent-appearing events occur with dis(78%). Commotio cordis resulting from blows to proportionate frequency in the youngest known the chest from projectiles (predominantly base- victims (10 years old or younger), with close famballs, softballs, lacrosse balls, or hockey pucks) ily members (e.g., parents or siblings) or friends or blunt bodily contact with other athletes are often responsible for the blow. In one example, a most common in children younger than 15 years child playing catch with a parent misjudged the of age. flight of the ball, which was then deflected off Although cardiovascular collapse is virtually his glove, striking his chest. In recreational sports,
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Table 1. Examples of Circumstances in Which Chest Blows Have Triggered Commotio Cordis. Sports Baseball, softball, cricket Batter struck by a pitched ball Batter hit by pitched ball while attempting to bunt Pitcher hit by a batted or thrown ball Base runner hit by a batted or thrown ball while running or sliding Player inadvertently in path of thrown or batted ball Catcher, umpire, spectator, or bystander hit by a foul ball Batter on deck hit by an errant throw Catcher struck by a bat Fielders or base runners involved in bodily collision Fielder hit when flight of ball was misjudged and ball deflected off glove Player fell on softball after catching it Player hit by bowled cricket ball Football Player hit in bodily collision with opponents helmet, forearm, shoulder, or knee, usually during blocking or tackling or after pass reception Player struck by ball while blocking punt Soccer Player collided with goalpost Goalie struck by shot on goal Player kicked in chest by opponent Hockey Goalie or other defensive player struck by shot on goal Player hit in bodily collision involving checking Player struck by slap shot hockey puck traveling at high speed Player struck by hockey stick Lacrosse Goalie hit by high-velocity shot on goal Player hit by ball passed from teammate Fights and scuffles, with blow from hand or elbow Psychiatric aide struck by patient Teacher struck while restraining student during fight Youth struck during play shadowboxing or roughhousing Youth struck by boxing glove during sparring Child struck by parent or babysitter (with disciplinary intent) Young adult struck during slam dancing Student involved in fist fight at fraternity party Youth hit by snowball Adult struck in prison gang initiation ritual Infant struck with open hand while having diaper changed Other circumstances Child kicked by horse Youth hit with recoil of gun butt while deer hunting Child hit with rebound of playground swing Adult thrown against steering wheel during automobile accident Youth hit by tennis ball filled with coins Young adult kicked during cheerleading routine Adult received chest blow by falling into body of water Child received blow from head of 23-kg (50-lb) pet dog Child received blow from falling on playground apparatus Child hit by tossed hollow plastic bat Child hit by plastic sledding saucer Youth received blow intended to terminate hiccups Child hit handlebars while falling off bicycle

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the speed of the projectiles causing chest blows ranges widely, from the low-velocity balls thrown during informal games of catch to high-velocity lacrosse or cricket balls.
Other Activities

Commotio cordis is unrelated to sports activities in about 25% of victims (most often the youngest) (Fig. 1). These incidents occur in a wide variety of circumstances, such as being kicked in the chest by a horse or struck by a playground swing as it rebounds. On occasion, such accidents are Mech a nisms brought to court. Charges of murder or manslaughter have led to criminal prosecution and Commotio cordis is a primary arrhythmic event incarceration.45-49 that occurs when the mechanical energy generated by a blow is confined to a small area of the precordium and profoundly alters the electrical Ou t c ome stability of the myocardium, resulting in ventricCommotio cordis is usually, although not invari- ular fibrillation. A variety of biologic and biomeably, fatal.1,2,19,50,51 In only about 25% of the chanical experimental models of commotio cordis cases reported in the Minneapolis registry has have been developed to elucidate the mechanisms cardiopulmonary resuscitation or defibrillation by which a rapid mechanical stimulus to the chest resulted in survival a low percentage, consider- triggers ventricular fibrillation.3,4,8,20,25-29,34,35,53-55 ing that commotio cordis is defined by the ab- Early efforts, dating back to the late 19th century, sence of structural heart disease. The outcome is to replicate commotio cordis in animals were related largely to the circumstances in which relatively crude, making use of hammers and commotio cordis occurs. Deaths have often been other blunt instruments that often resulted in associated with the failure of bystanders to ap- death from direct trauma.3,4,8,9 These early invespreciate the life-threatening nature of the collapse tigations yielded several theoretical explanations and to initiate appropriately aggressive and timely for the mechanics of the event, including excesmeasures of resuscitation.2,17 sive autonomic (vagal) reflex6,8,9 and coronary Registry data show that survival rates have arterial vasospasm,3,4,6,8 that have since been increased over time, rising to 35% over the past abandoned. During testing in later models, basedecade, as compared with 15% for the preceding balls were propelled at speeds of up to 153 km 10 years (P=0.01); most recently between 2006 (95 mi) per hour, causing severe injuries to the and 2009 the number of successful resuscita- thorax and heart (cardiac contusion) but not tions exceeded the number of deaths by 20%. commotio cordis.53 This improvement is probably the result of increased public awareness, the increased availabil- Determinants and Triggers ity of automatic external defibrillators (AEDs), More recent experimental laboratory studies conand earlier activation of the chain of survival ducted under controlled conditions in pigs, dogs, (call to 911 and initiation of cardiopulmonary and rabbits20-27,29-35,53 have provided insights into resuscitation, defibrillation, and advanced life- the underlying mechanisms of commotio cordis support measures). Arrhythmias recorded at the that are consistent with its clinical profile and time of collapse or in the emergency room are have dispelled the notion that sudden death after often caused by ventricular fibrillation,2 suggest- a blow to the chest is a mysterious phenomeing that restoration of sinus rhythm and survival non.1,2 One model, in which projectile-induced are possible, given prompt defibrillation. blows were delivered at a wide range of velocities Some commotio cordis events may abort spon- to anesthetized young pigs in synchronization taneously, when the blow causes nonsustained with the cardiac cycle, revealed two critically imarrhythmias, although this is difficult to con- portant mechanical determinants of ventricular firm. Such cases have been recorded in the reg- fibrillation and lethality (Fig. 2).20,33
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istry, including the case of a professional hockey player who collapsed immediately after being struck in the chest by a puck traveling at high velocity. The players slow pulse suggested transient complete heart block (or another bradyarrhythmia), as has been reported in laboratory settings, in which a blow to the chest is timed to occur during the QRS complex20; the player regained consciousness spontaneously, within a few minutes after his collapse, and recovered.52

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Figure 2. Pathophysiology of Commotio Cordis. In recreational and competitive sports, chest blows may involve balls or pucks or may be inflicted through bodily contact. The location of the blow on the chest and its timing relative to the cardiac cycle are the primary determinants of commotio cordis. Other factors that may contribute to the risk of an event include the density, size, and orientation of the projectile and the shape of the thorax; younger people are the most vulnerable because of their thinner, less developed rib cage and musculature.

The first of these determinants involves the location of the blow, which must be directly over the heart (particularly at or near the center of the cardiac silhouette).20,33 This finding is consistent with clinical observations that precordial bruises representing the imprint of a blow are frequently evident in victims.1,2 There is no evidence in humans or in experimental models that blows sustained outside the precordium (e.g., the back, the flank, or the right side of the chest) cause sudden death.27,33 The second determinant concerns the timing of the blow, which must occur within a narrow window of 10 to 20 msec on the upstroke of the T wave, just before its peak (accounting for only 1% of the cardiac cycle) that is, the blow must occur during an electrically vulnerable period,

when inhomogeneous dispersion of repolarization is greatest, creating a susceptible myocardial substrate for provoked ventricular fibrillation (Fig. 2).20 In pigs, when blows occurred outside this brief window of time, ventricular fibrillation was not the consequence; instead, what followed was transient complete heart block, left bundlebranch block, or ST-segment elevation.20 These effects have also been reported in some human survivors (with the presumed timing of the blow coinciding with the QRS complex during ventricular depolarization).12,50 The energy of the impact associated with commotio cordis is not uniform, characteristically encompassing a wide range of velocities as well as projectile sizes, shapes, and weights. Projectiles include hockey pucks and lacrosse balls
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propelled at speeds of up to 145 km (90 mi) per hour,1,2 as well as seemingly innocuous objects, such as plastic toy bats and sledding saucers, that can become lethal when striking small children, even at slow speeds. Under experimental conditions, the likelihood that ventricular fibrillation will be triggered by a projectile the size of a baseball increases progressively up to an impact velocity of 64 km (40 mi) per hour, a speed typically delivered by 11- and 12-year-old pitchers.24 At higher velocities (exceeding 80 km [50 mi] per hour), there is an increased risk of structural damage to the chest and heart, including myocardial bruising and rupture that are characteristic of cardiac contusion (rather than commotio cordis).24,53 Other factors that may increase the risk of ventricular fibrillation and commotio cordis include the hardness of the object and its size and shape, with hard, small, sphere-shaped projectiles most likely to do harm.20,23,56 The predisposition to commotio cordis in young people may largely be related to physical characteristics of the thorax in the young33,56; the relatively thin, underdeveloped, compliant chest cage (and immature intercostal musculature) is less capable of blunting the arrhythmogenic consequences of precordial blows.1,2 In addition, since children probably incur chest blows more frequently than adults in a variety of circumstances, they may generally be at greater risk for commotio cordis. Adults probably gain a measure of protection from their mature and fully developed chest cage, which may explain in part the apparently low rate of commotio cordis events in sports such as kickboxing and boxing (accounting for less than 5% of registry cases). In boxing, it is also possible that the glove itself, which increases the area of impact, helps to buffer the force of the blow.2 The question of whether susceptibility to commotio cordis varies because of individual variations in the length of the QT interval has been considered but remains unanswered. There is no evidence that survivors of commotio cordis are at increased risk for subsequent arrhythmic events, nor is there evidence that athletes who have had a commotio cordis event should be disqualified from competition solely for that reason. Similarly, prophylactic implantable defibrillators are not indicated for persons who have survived commotio cordis in the absence of cardiac disease.
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Cellular Mechanisms

The cellular (and subcellular) mechanisms responsible for commotio cordis appear to be multifactorial and complex, and they remain incompletely defined. Information obtained from experiments with Langendorff preparations of perfused rabbit heart27 and from animal models21,24,30-32 has led to hypotheses concerning specific mechanistic pathways. It is believed that the mechanical force generated by precordial blows during repolarization causes left ventricular intracavitary pressure to rise instantaneously to 250 to 450 mm Hg; this rise in pressure is directly correlated with an increased probability of ventricular fibrillation.21,24,27,33 It has been hypothesized that this elevation in pressure causes cell membranes to stretch, activating ion channels and increasing transmembrane current flow by means of mechanicalelectric coupling.21,26,27,29,30,35 The resultant amplified dispersion of repolarization creates an inhomogeneous and electrically vulnerable substrate that is susceptible to ventricular fibrillation. The candidate ion channels include the ATP-sensitive potassium channel,26 which contributes to the initiation of ventricular fibrillation in commotio cordis21 and in myocardial infarction and ischemia.57-62 It is possible that the mechanism by which ventricular fibrillation occurs in commotio cordis, with ventricular depolarization induced by a blow to the chest, has something in common with the pathophysiological mechanisms that give rise to primary arrhythmogenic conditions, such as ion channelopathies.63-68

Pr e v en t i v e S t r ategie s a nd F u t ur e C onsider at ions


Primary Prevention

The risk of commotio cordis is associated with lifestyle and therefore can be modified. One means of prevention is public education people should be made aware of the importance of avoiding precordial blows.56 It is particularly important to increase awareness that even an unintentional, modest-seeming blow to the chest delivered without malice (e.g., in playful boxing) can trigger life-threatening ventricular tachyarrhythmias.2 Even so, since there are so many circumstances in which commotio cordis can occur (Table 1), elimination of these events is an unrealistic goal. Organized sports present the greatest oppor-

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tunity to prevent commotio cordis. For example, the risk would probably be reduced by means of improved coaching techniques, such as teaching inexperienced young batters in baseball and softball how to turn away from the ball to avoid errant pitches.56,69 Defensive players in lacrosse and hockey can be coached to avoid using their chest to block the ball or puck when protecting their goal. Coaching clinics sponsored by the National Collegiate Athletic Association now strongly discourage any tactic that places lacrosse players (who are not goalies) directly in the path of shots on goal. Improved design of commercial sports equipment would also probably help to prevent commotio cordis. One example is the safety baseball, a softer ball intended for players younger than 13 years of age; the safety baseball is made entirely of rubber, without the dense, hard core of cork and twine found in standard baseballs. A direct relation between the hardness of the ball and the likelihood of ventricular fibrillation has been demonstrated in the laboratory, and lethal arrhythmias occur less frequent ly when the balls used have been manufactured for reduced hardness.20,23,56 However, softer balls will not be accepted if they change the nature of the game, and their absolute effectiveness in reducing the risk of commotio cordis has not been documented in the field. In fact, so-called safety baseballs have been responsible for several fatal events.2 The observation that the air-filled balls used in soccer, tennis, and basketball are rarely implicated in commotio cordis (accounting for only 4% of projectile-related deaths, according to the Minneapolis registry) is consistent with the principle that solid projectiles are more likely to precipitate ventricular fibrillation; air-filled balls are presumed to be safer because of their propensity to collapse, or give, on contact and to absorb some of the energy of the impact. Chest protectors and vests have been a focus for primary prevention of commotio cordis in certain sports.34,54,56,70,71 However, registry data indicate that the most commonly used, commercially available protectors, which were originally designed to reduce the likelihood of trauma from blunt bodily injury but not to provide protection against commotio cordis do not offer absolute protection from arrhythmia after a blow to the chest.1,2,19,70 Indeed, currently available chest protectors may create a false sense of secu-

rity, given that almost 20% of the victims of commotio cordis in competitive football, baseball, lacrosse, and hockey were wearing equipment marketed as providing protection against traumatic chest injury (Fig. 3).1,2,9,70,72 In several fatal cases of commotio cordis in lacrosse goalies, the ball struck the chest protector directly.19 Such cases suggest that the material the protectors were made from was inadequate. In other cases of commotio cordis, a flawed design of the chest barrier allowed the projectile direct access to the precordium. For example, in hockey, when a players arms are fully raised, the protector can migrate upward, exposing the chest wall to a direct blow.1,70,72 Confirmatory evidence from animal models indicates that the commercially produced chest protectors now promoted for use in baseball and lacrosse are ineffective in consistently preventing ventricular fibrillation that is, wearing such protectors does not reduce the risk of sudden death.25,34 Development of a chest barrier that is adequately designed to prevent commotio cordis during sports competition may prove difficult. To be effective, a chest protector would have to absorb and dissipate the energy generated by the precordial impact.56 In laboratory studies, a mechan ical model that could diffuse the force of chest blows over an increased surface area was most effective in preventing commotio cordis.54 Furthermore, both clinical observations1,2,19 and laboratory data25,34,70 suggest that closed-cell foam, which is the primary constituent of most commercially available chest protectors, is easily penetrated by projectiles and does not provide adequate protection against commotio cordis. It is likely that chest protectors would be more effective if they were made from harder, more rigid, and more resistant materials and from foams capable of absorbing and dispersing greater amounts of energy. In practical design terms, such a chest protector should be adaptable for use by athletes playing any position in any sport in which there is a risk of commotio cordis; currently, the use of such protectors is largely limited to goalies in lacrosse and hockey and to catchers in baseball, positions that have been associated with 20% of all commotio cordis events.70 An ideal chest-wall protector would also have to be affordable, durable, and compatible with the full range of physical activity and comfort required by athletes in a given sport and
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Total cases 224

Recreational sports or other circumstances

99 Chest protector

125 Competitive sports No chest protector 58 9 40 85 7 1 Baseball or softball Soccer Lacrosse Hockey Other sports

17 Hockey

14 Football

5 Baseball

4 Lacrosse

10

Figure 3. Means of Protection from Commotio RETAKE: 1st AUTHOR: Maron Cordis. Commercially available chest protectors have proved inadequate in the prevention 2nd of sudden death due to commoFIGURE: 3 of 3 3rd tio cordis. Reasons for the inadequacy include the fact that the protector may move when the arms are raised, leavRevised 1,72 or that ing the precordium exposed (as ARTIST: in the case MRLof the protector shown in Panel A, which is used in hockey), SIZE the composite material the protector is made from does not adequately attenuate the blow (as in the case of the 6 col Combo 4-C 25H/T 33p9 (Panel C), made with rubber protector shown in Panel B, whichTYPE: is used Line by baseball catchers). Softer baseballs cores rather than the standard-issue cork and twine, intended avert commotio cordis events in children, have AUTHOR, PLEASEto NOTE: Figure has been redrawn and type has been reset. on data derived from the 224 fatal nonetheless been responsible for such events. A flow diagram (Panel D) based Please check carefully. cases of commotio cordis recorded in the National Commotio Cordis Registry shows that in competitive sports, almost one third (40 of 125) ofJOB: the athletes who died as a result of the event were wearing a chest barrier. Other 361xx ISSUE: 3-11-10 sports include boxing, cricket, equestrian competition, karate, and rugby.

would have to meet prespecified performance in terminating life-threatening ventricular tachy standards.54 arrhythmias and restoring sinus rhythm.2,69,74,75 Indeed, AEDs have also effectively terminated Secondary Prevention ventricular fibrillation in animal models of AEDs have substantial life-saving capability, and commotio cordis.22 However, even under optiit is appropriate to disseminate them widely at mal conditions, an AED can fail to restore the youth sporting events and recreational settings heart to normal rhythm after commotio cordis, where commotio cordis may occur.73 A public as was the case with a college lacrosse player health strategy that incorporates a plan for making who was not a goalie but was struck in the chest AEDs widely available is likely to result in the sur- by a ball and died, despite particularly prompt vival of more young people in the event of com- efforts at resuscitation and defibrillation.76 Both motio cordis, as indicated by current registry data clinical studies77-81 and experimental studies82 and several cases in which an AED was effective suggest that precordial thumps are unreliable in
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terminating ventricular fibrillation caused by chest motio cordis events. Further efforts are needed blows. to prevent these largely avoidable deaths by providing more education, better-designed athletic equipment (e.g., effective chest-wall protectors), Sum m a r y and wider access to AEDs at organized athletic In the past decade, the general public and the events. These strategies should result in a safer medical community have become more aware of sports environment for our youth. commotio cordis as an important cause of sudSupported in part by grants from the Hearst Foundations, the den death. Commotio cordis occurs in otherwise Louis J. Acompora Memorial Foundation, and the National Ophealthy and active young people, typically during erating Committee on Standards for Athletic Equipment. Dr. Maron reports receiving consulting fees from GeneDx (a recreational and competitive sports but in some subsidiary of Bio-Reference Laboratories) and lecture fees and cases even during normal daily activities. A variety grant support from Medtronic. Dr. Estes reports that his instituof experimental models indicate that if delivered tion has received fellowship funding from St. Jude Medical, at a particular moment in the cardiac cycle, even Boston Scientific, and Medtronic and that he has received lecture fees and travel support from Boston Scientific. innocent-appearing precordial blows can trigger We thank David Mottet for his assistance with an earlier verventricular fibrillation and result in fatal com- sion of Figure 2.
References
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